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Immunology Y5 > Case studies in immunology > Flashcards

Case studies in immunology Flashcards

1
Q

Basic pathophysiology of anaphylaxis

A
  • Type I hypersensitivity response
  • Previously sensitised to the allergen
  • Re-exposure → cross-linking of IgE on the surface of mast cells
  • This causes mast cells to degranulate
  • This results in the release of specific biological mediators including histamines and leukotrienes
  • This results in:
    • Increased vascular permeability
    • Smooth muscle contraction
    • Inflammation, increased mucus production
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2
Q

Common causes of anaphylaxis

A
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3
Q

Most commom features of anaphylaxis

A

Urticaria and angiooedema

followed by upper airway oedema

***usually do get skin manifestations **

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4
Q

Management of anaphylaxis

A
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5
Q

What is Latex?

A

milky fluid produced by rubber trees (Hevea brasiliensis

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6
Q

What are the two types of hypersensitivity reactions you can get with latex?

A
  1. Type 1
    - IgE mediated
    - immediate
    - cross-reactive with certain fruits (Latex fruit allergy syndrome) - BAACK
  2. Type 4
    - contact dermatitis
    - 24-48 hours after exposure
    - usually affects hands and feet
    - usually due to rubber additives rather than latex itself
    - unresponsive to antihistamines as it’s not mediated by histamine
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7
Q

Investigations for latex allergy

A
  • skin prick testing (in vivo)
  • patch testing (in vivo)

- specific IgE - preferable in patients with a history of anaphylaxis. but poor sensitivity and specificity.

- component individual allergen test: higher sensitiivty

  • challenge test - if inconclusive skin prick or blood test

Trend: skin, blood, challenge

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8
Q

What allergies does desensitisation work for?

A
  • insect venom
  • some aeor-allergens eg pollen

**not latex **

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9
Q

What disorders are associated with recurrent meningococcal meningitis?

A
  1. complement deficiency - susceptibility to encapsulated bacteria
  2. antibody deficiency- susceptibility to bacterial infections, esp. upper and lower respiratory tract

**but also neurological disorders such as skull fracture**

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10
Q

Factors that imply immunodeficiency

A
  1. Serious infections (from innocuous/ harmless organisms)
  2. Persistent infections- e.g. resistant to Abx Tx
  3. Unusual
    • Unusual organisms
    • Opportunistic organisms
    • Unusual sites of infection- deep muscle abscesses
  4. Recurrent minor infections

Concomitant problems:

  • Failure to thrive
  • Family history
  • History of autoimmune diagnosis, malignancy etc.
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11
Q

How does the CH50 test work?

A
  • CH50 is a functional test of the integrity of the whole CLASSICAL complement cascade
  • Classical pathway is activated by Ab bound to antigen
  • The CH50 test uses antibody-coated sheep RBC
  • If classical pathway is working, those RBC will be lysed
  • So you mix patient’s serum with the preparation of antibody-coated sheep RBC
  • Test measures the haemolysis by the release of Hb
  • Positive/ normal test = good amount of haemolysis
    • Note: ALL components of the cascade (classical pathway and final common pathway) need to be in place for the test
    • → membrane attack complex → haemolysis
    • → give a positive (NORMAL) result
    • Low/ absent haemolysis = immunolgical problem - complement deficiency
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12
Q

How does the AP50 test work?

A
  • AP50 is a functional test of the integrity of the whole ALTERNATIVE complement cascade
  • Uses rabbit RBC which has a coating that is not protected from complement lysis using the alternative pathway
  • Mix rabbit RBC and patient’s serum
  • If alternative pathway works → membrane attack complex → haemolysis of rabbit RBC
  • Positive result = good amount of haemolysis (normal)
  • ALL components of the cascade (alternative and final common) need to be in place for the test to give a positive (NORMAL) result
  • Low/ absent haemolysis = immunolgical problem - complement deficiency
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13
Q

NORMAL C3 and C4

Absent CH50

Absent AP50

A

Defect of final common pathway

C5, C6, C7, C8, C9

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14
Q

Why can’t you give patients complement for complement deficiency

A

because complement protein is labile

Instead- you give: vaccinations against encapuslated bacteria and daily prophylactic penicilin

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15
Q

Which immunologicla defect increases susceptibility to meningococcal disease?

A

Any complement deficiency but especially alternative pathway or final common pathway defect

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16
Q

SLE antibodies

A

Anti ds-DNA: most specific

Anti-Ro, anti-La, anti-Sm, anti-RNP: not specific

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17
Q

Limited cutaneous systemic sclerosis (CREST syndrome) antibodies

A

Anti-centromere

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18
Q

Diffuse systemic sclerosis antibody (scleroderma)

A

anti-topoisomerase - anti-SCL 70

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19
Q

Sjogren’s antibodies

A

Anti Ro

Anti La

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20
Q

Myositis antibodies

A

anti-Jo1 (type of tRNA synthetase)

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21
Q

Types of ANA antibodies

A
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22
Q

What suggests SLE is active?

A

Low C3 and C4

Also can monitor disease activity with ESR and anti-ds DNA antibody

**but need to correlate with clinical picture

23
Q

Renal biopsy of lupus nephritis vs goodpasture’s

A

Lupus nephritis: lumpy bumpy (grnaular) deposition of immune complexes

*diffuse prolfierative nephritis is the most common pattern foudn in the kidneys

Goodpastures: linear deposition of antibodies at the glomerular basement membrane

24
Q

Two main regions affected by SLE

A

joints and kidney

25
Q

Drugs useful for treatment of SLE

26
Q

PBC antibody

A

Anti-mitochondrial antibody

29
Q

What is serum sickness?

A

Type III hypersensitivity (immune complex mediated) reaction to drugs like penicillin

key thing: involves a foreign protein rather than an autoantigen as in SLE

30
Q

Clinical manifestations of serum sickness

A

disorientation - because immune complexes lead to small vessel vasculitis in the blood vessels leading to the brain

31
Q

Investigations for serum sickness

34
Q

Investigations for immunodeficiency

A

FISH

FBC

Immunoglobulin

Serum c3 and c4 (complement)

HIV

35
Q

CD4 and CD8 T cells – present

B cells- very LOW numbers

Specific responses to tetanus/ HiB- NEGATIVE

A

Bruton’s X-linked agammaglobulinaemia

36
Q

What is Bruton’s X-linked agammaglobulinaemia

A

Deficiency of a tyrosine kinase needed for B lymphocyte maturation from bone marrow going out into circulation

Failure of pre-B cells to mature in the bone marrow → low B cell numbers

This leads to failure to produce immunoglobulins → Low Ab numbers

37
Q

Mx of bruton’s

A
  • pooled serum Ig
  • HSCT
38
Q

What is flow cytometry used for in. the context of immunodeficiency investgation?

A

To test for lymphoid markers to figure out which subset it is

39
Q
A

Bruton’s x linked agammaglobulinaemia

40
Q

Ddx?

A

Multiple myeloma (top differential)

Osteoporosis and Sjogren’s syndrome

Osteoporosis and SLE

***rmb, you can get recurrent infections in multiple myeloma because of bone marrow infiltration***

41
Q

What region of antibody determines class of antibody?

A

heavy chain

**light chain determines the specificty for diff antigens as it’s found in the antigen binding region

42
Q

Multiple myeloma tests

A

1. serum imuunoglobulins

2. serum protein electrophoresis - looking at HEAVY chain to see whether monoclonal band

  • can be negative

3. urinary bence jones protein - looking at LIGHT chain

  • need to do this because in 75% of patients with MM you don’t get monoclonal band on serum electrophoresis
    (4) x-ray : punched out lytic lesions
43
Q

Why do you get recurrent infections in multiple myeloma?

Why do you get anaemia in multiple myeloma?

Why is ESR raised?

A

Recurrent infections

  • there’s suppression of normal immunoglobulin by the malignant clone
  • → results in a functional antibody deficiency
  • This is sometimes called immune paresis

Anaemia

  • Expansion of malignant clone of plasma cells
  • → crowds out the normal RBC and WBC precursors in the bone marrow
  • The tumour may produce local cytokines which inhibits normal bone marrow function

Raised ESR

  • ESR = measure of the rate of fall of erythrocytes through plasma
  • Normally, erythrocytes do NOT clump
    • because the repellent negative surface charge is greater than the attractant charge of plasma constituents
  • However, if the protein constituents of plasma increase/ change:
    • Increases attractant charge
      • Causes erythrocytes to clump together
    • Clumped erythrocytes fall more quickly
    • This results in a raised ESR
44
Q

ESR and CRP in rheumatoid arthritis and SLE

A

RA: ESR and CRP both raised

SLE: ESR raised, CRP normal

45
Q

RF antibodies

A

RF

Anti-CCP- specific

46
Q

What is a common trigger for rheumatoid arthritis?

A

Post-partum presentation is common

Due to change in T-cell phenotype from Th2 to Th1 after delivery

47
Q

What is Rheumatoid Factor? Why is it not diagnostic of rheumatoid arthritis?

A

IgM (usually) antibodies are directed against the Fc region of human IgG

  • Assays look for the IgM RF although patients may also have IgG and IgA RF
  • RF is not very specific to Rheumatoid Arthritis
  • Approximately 60-70% sensitive and specific (found in other diseases)
49
Q

Genetic associations of rheumatoid arthritis

A
  1. HLA associations

HLA DR1

HLA DR 4

  1. PAD Type 2 and 4
  2. PTPN22
50
Q

Management of rheumatoid arthritis

A

TNF alpha antagonists- infliximab, etanercept

51
Q

Name an anti CTLA4 agent

52
Q

Pathognemonic features of rhematoid arthritis

53
Q

Key cytokines in rheumatoid arthritis - targeted by drugs

A
  1. IL6
  2. TNF Alpha - produced by macrophages

(IL1 is another minor cytokine)

Immunology Y5 (11 decks)

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